Worldwide variability in growth and its association with health: Incorporating body composition, developmental plasticity, and intergenerational effects

Abstract

In their seminal book "Worldwide variation in human growth," published in 1976, Eveleth and Tanner highlighted substantial variability within and between populations in the magnitude and schedule of human growth. In the four decades since then, research has clarified why growth variability is so closely associated with human health. First, growth patterns are strongly associated with body composition, both in the short- and long-term. Poor growth in early life constrains the acquisition of lean tissue, while compensatory "catch-up" growth may elevate body fatness. Second, these data are examples of the fundamental link between growth and developmental plasticity. Growth is highly sensitive to ecological stresses and stimuli during early "critical windows," but loses much of this sensitivity as it undergoes canalization during early childhood. Crucially, the primary source of stimuli during early "critical windows" is not the external environment itself, but rather maternal phenotype, which transduces the impact of ecological conditions. Maternal phenotype, representing many dimensions of "capital," thus generates a powerful impact on the developmental trajectory of the offspring. There is increasing evidence that low levels of maternal capital impact the offspring's size at birth, schedule of maturation, and body composition and physiological function in adulthood. While evidence has accrued of substantial heritability in adult height, it is clear that the pathway through which it is attained has major implications for metabolic phenotype. Integrating these perspectives is important for understanding how developmental plasticity may on the one hand contribute to adaptation, while on the other shape susceptibility to non-communicable disease.

Foetal and childhood exposure to famine and the risks of cardiometabolic conditions in adulthood: A systematic review and meta‐analysis of observational studies

“…In this case, early‐life nutrition has been increasingly recognized as an important determinant of lifelong health risk . It has been postulated that poor foetal nutrition can trigger an adaptive response to enhance survival in a sparse nutritional environment . However, if the individuals are subsequently exposed to adequate nutrition or overnutrition in later life, these adaptive responses may increase susceptibility to the development of cardiometabolic conditions in adulthood .…”

“…It has been postulated that poor foetal nutrition can trigger an adaptive response to enhance survival in a sparse nutritional environment . However, if the individuals are subsequently exposed to adequate nutrition or overnutrition in later life, these adaptive responses may increase susceptibility to the development of cardiometabolic conditions in adulthood . Indeed, epidemiological evidence has linked low birth weight, marker indicative of foetal undernutrition, to susceptibility to type 2 diabetes mellitus (T2DM), metabolic syndrome, hypertension, and coronary heart disease later in life.…”

Parents of early‐maturing girls die younger

“…Individual‐level associations between lifespan and rate of sexual maturation may reflect either within‐population polymorphisms in antagonistic pleiotropic effects (Corbett, Courtiol, Lummaa, Moorad, & Stearns, ; Laisk et al, ) or induced phenotypic responses to womb or childhood environment (Lea, Tung, Archie, & Alberts, ; Wells, ). For instance, the risk of developing diseases related to metabolic syndrome among early‐maturing women might appear inevitable consequence of (initially adaptive) plastic response of a “thrifty phenotype” to low maternal investment in utero (Wells, ), but also result from the overlap of genomic loci associated with early menarche with genes implicated in metabolic diseases (Day et al, ; Perry et al, ).…”

“…Individual‐level associations between lifespan and rate of sexual maturation may reflect either within‐population polymorphisms in antagonistic pleiotropic effects (Corbett, Courtiol, Lummaa, Moorad, & Stearns, ; Laisk et al, ) or induced phenotypic responses to womb or childhood environment (Lea, Tung, Archie, & Alberts, ; Wells, ). For instance, the risk of developing diseases related to metabolic syndrome among early‐maturing women might appear inevitable consequence of (initially adaptive) plastic response of a “thrifty phenotype” to low maternal investment in utero (Wells, ), but also result from the overlap of genomic loci associated with early menarche with genes implicated in metabolic diseases (Day et al, ; Perry et al, ). Similarly, early maturation of girls growing up without father present in the family may appear a predictive response to cues of environmental harshness or uncertainty that favours switching to a precocious life‐history strategy (Belsky, Steinberg, & Draper, ; Ellis, ) or simply a result of genetic coupling between propensity towards behaviours leading to divorce (and/or early death) and fast sexual maturation (Comings, Muhleman, Johnson, & MacMurray, ).…”

Short Maternal Stature and Increased Risk of Ischaemic Placental Disease: Is the Association Driven by Unmeasured Confounding?

“…Evaluating height as a marker of human health assumes that optimal height is the genetically pre‐programmed growth to which the individual would be destined to reach under ideal circumstances. Unexpectedly shorter maternal height could therefore represent exposure to sub‐optimal conditions, either in utero or during childhood or adolescence, that prevented the individual from reaching her full growth potential …”